Daneshvar Daniel H, Goldstein Lee E, Kiernan Patrick T, Stein Thor D, McKee Ann C
Boston University Chronic Traumatic Encephalopathy Program, Boston University School of Medicine, 72 E. Concord St., Boston, MA 02118, USA; Boston University Alzheimer's Disease Center, Boston University School of Medicine, 72 E. Concord St., Boston, MA 02118, USA; Department of Neurology, Boston University School of Medicine, 72 E. Concord St., Boston, MA 02118, USA.
Boston University Chronic Traumatic Encephalopathy Program, Boston University School of Medicine, 72 E. Concord St., Boston, MA 02118, USA; Boston University Alzheimer's Disease Center, Boston University School of Medicine, 72 E. Concord St., Boston, MA 02118, USA; Department of Neurology, Boston University School of Medicine, 72 E. Concord St., Boston, MA 02118, USA; Department of Pathology and Laboratory Medicine, Boston University School of Medicine, 72 E. Concord St., Boston, MA 02118, USA; Department of Pharmacology & Experimental Therapeutics, Boston University School of Medicine, 72 E. Concord St., Boston, MA 02118, USA; Department of Neurosurgery, Boston University School of Medicine, 72 E. Concord St., Boston, MA 02118, USA; Boston University Photonics Center, Boston University, 1 Silber Way, Boston, MA 02115, USA; Department of Biomedical Engineering, Boston University, 1 Silber Way, Boston, MA 02115, USA; Department of Electrical and Computer Engineering, Boston University, 1 Silber Way, Boston, MA 02115, USA; Department of Mechanical Engineering, Boston University, 1 Silber Way, Boston, MA 02115, USA.
Mol Cell Neurosci. 2015 May;66(Pt B):81-90. doi: 10.1016/j.mcn.2015.03.007. Epub 2015 Mar 7.
Traumatic brain injury (TBI) is a leading cause of mortality and morbidity around the world. Concussive and subconcussive forms of closed-head injury due to impact or blast neurotrauma represent the most common types of TBI in civilian and military settings. It is becoming increasingly evident that TBI can lead to persistent, long-term debilitating effects, and in some cases, progressive neurodegeneration and chronic traumatic encephalopathy (CTE). The epidemiological literature suggests that a single moderate-to-severe TBI may be associated with accelerated neurodegeneration and increased risk of Alzheimer's disease, Parkinson's disease, or motor neuron disease. However, the pathologic phenotype of these post-traumatic neurodegenerations is largely unknown and there may be pathobiological differences between post-traumatic disease and the corresponding sporadic disorder. By contrast, the pathology of CTE is increasingly well known and is characterized by a distinctive pattern of progressive brain atrophy and accumulation of hyperphosphorylated tau neurofibrillary and glial tangles, dystrophic neurites, 43 kDa TAR DNA-binding protein (TDP-43) neuronal and glial aggregates, microvasculopathy, myelinated axonopathy, neuroinflammation, and white matter degeneration. Clinically, CTE is associated with behavioral changes, executive dysfunction, memory deficits, and cognitive impairments that begin insidiously and most often progress slowly over decades. Although research on the long-term effects of TBI is advancing quickly, the incidence and prevalence of post-traumatic neurodegeneration and CTE are unknown. Critical knowledge gaps include elucidation of pathogenic mechanisms, identification of genetic risk factors, and clarification of relevant variables-including age at exposure to trauma, history of prior and subsequent head trauma, substance use, gender, stress, and comorbidities-all of which may contribute to risk profiles and the development of post-traumatic neurodegeneration and CTE. This article is part of a Special Issue entitled 'Traumatic Brain Injury'.
创伤性脑损伤（TBI）是全球范围内导致死亡和发病的主要原因。因撞击或爆炸性神经创伤导致的闭合性头部损伤的震荡性和亚震荡性形式是 civilian 和军事环境中最常见的 TBI 类型。越来越明显的是，TBI 可导致持续的、长期的衰弱性影响，在某些情况下，还会导致进行性神经退行性变和慢性创伤性脑病（CTE）。流行病学文献表明，单次中度至重度 TBI 可能与神经退行性变加速以及患阿尔茨海默病、帕金森病或运动神经元病的风险增加有关。然而，这些创伤后神经退行性变的病理表型在很大程度上尚不清楚，创伤后疾病与相应的散发性疾病之间可能存在病理生物学差异。相比之下，CTE 的病理学越来越为人所知，其特征是进行性脑萎缩的独特模式以及过度磷酸化的 tau 神经原纤维和胶质缠结、营养不良性神经突、43 kDa TAR DNA 结合蛋白（TDP - 43）神经元和胶质聚集物、微血管病变、有髓轴索病变、神经炎症和白质变性的积累。临床上，CTE 与行为改变、执行功能障碍、记忆缺陷和认知障碍有关，这些症状隐匿起病，大多在数十年间缓慢进展。尽管对 TBI 长期影响的研究进展迅速，但创伤后神经退行性变和 CTE 的发病率和患病率尚不清楚。关键的知识空白包括阐明致病机制、识别遗传风险因素以及澄清相关变量，包括创伤暴露时的年龄、既往和随后头部创伤史、物质使用、性别、压力和合并症，所有这些都可能影响风险特征以及创伤后神经退行性变和 CTE 的发展。本文是名为“创伤性脑损伤”的特刊的一部分。
